Thursday, May 31, 2007

Recent research on behavioral characteristics displayed by anorexia nervosa (AN) and anorexia nervosa recovered (ANR) patients point strongly towards an anomalous pattern of activation of the pre-frontal cortex. Unlike in normal women, where food triggers off a reward system in the brain, AN and ANR (those who have recovered from anorexia nervosa) patients display an exaggerated startle effect, as part of an intrinsic defense reaction. In addition, they often salivate less, eat slower, and have a lower preference for fatty and sweet food, suggestive of a disruption in the central food-associated reward pathways.

Animal models of AN show that both extreme under-eating and binge eating may result in a disruption of the normal brain chemicals associated with ‘reward’, by an unregulated flooding of dopamine, opioids and cannabinoids in the brain. In a positron emission tomography (PET) study of brain scans in AN patients in 2005, a markedly reduced 5-HT receptor binding was confirmed, in the ‘punishment’ center in the cingulate region. This is thought to lead to a heightened sensitivity to ‘punishment’, and explains the basic food aversion in all types of AN. On the other hand, a variability of the sensitivity of the opposing reward systems lead to dramatic opposites in behavior - from extreme starvation to bingeing.

Current research also focuses on associations of distinct personality traits of AN/ANR patients. Weak set shifting (an ability to switch between mental tasks) is thought to be a core component of AN/ANR, and although it is seen in bipolar disorders and schizophrenia, its importance lies in its link with ‘reward’ sensitivities through variable effects on the dopaminergic pathways. In addition, AN/ANR patients show a bias towards detail in their tasks, although they display weakness in global processing, described as ‘weak central coherence’, a trait shared with autism and Asperger’s syndrome. Although they perform well in learning with effort, they are deficient in incidental or unconscious learning, which explains why AN/ANR patients are often poor at adapting to the demands of their work or social environment.

Finally, as the genetic correlates of AN/ANR are becoming clearer, population studies estimate the increase in familial risk to be by a factor of 10. The linkage to chromosome 1 is thought to determine anomalies in 5-HT genes, seen in restrictive AN subtypes (under-eaters). The other aspect of AN/ANR that has a familial clustering, is obsessive-compulsiveness (often leading to traits of perfectionism and undue concern with mistakes).

By the time early humans (Homo erectus,archaic Homo sapiens, Neanderthal Man, and the rest) first reached temperate Europe, at least 500,000 years ago, their diet clearly included a large amount of meat. We know this both archaeologically (for instance, by studying animal refuse at archaeological sites), and anatomically - with their large brains and small guts, these people needed to run on high-quality fuel. Moreover, according to work by the American anthropologists Thomas Berger and Erik Trinkaus, the Neanderthals had high rates of injury involving skeletal trauma most like that seem in modern rodeo performers - suggesting, they say, `frequent close encounters with large ungulates [ie, hoofed animals] unkindly disposed to the humans involved'.

But what we don't see at this time is evidence of overhunting - that is, an increase in the rate at which European herbivore species went extinct. If anything, after about 450,000 years ago, there seems to be an increase in herbivore diversity in Europe, and this is particularly marked among the rhinos, large bovids (cattle), ovicaprids (sheep and goats) and antelopes.

One of the reasons to blame low human population densities and poor hunting technology for this increase in animal biodiversity - rather than some `instinct for conservation' - is that when anatomically modern humans evolved later, armed with a more efficient hunting technology, more extensive social networks (we believe) and bigger hunting-group sizes, their impact on species biodiversity was marked - with some of the most notable evidence coming from the Americas.

Anatomically modern humans arrived in the Americas at the end of the last Ice Age 13,000- 14,000 years ago, and their arrival coincided with a peak in the extinction rates of endemic large animal species. At the end of the Ice Age in North America, 33 genera (or individual species) were lost, including several families of species, and one whole order (the mammoths and mastodons). In South America during the same period, at least 46 genera became extinct, including sloths, giant rodents, large carnivores, mastodons, horses, and various types of peccary (South American hogs), camel and deer.

Some of these extinctions must have been caused by indirect effects of human actions - removal of some large-bodied herbivores, for example, may have had knock-on consequences for other species. Some were surely due to the rapid climate changes of that time, altering ground vegetation cover at rates which may have outstripped the ability of many animals to adapt or migrate. But in cases such as the mammoths, mastodons, ground sloths, horses, camels and giant tortoises, where remains of extinct species have been found in association with Early Palaeoindian artefacts, a role for human predation seems undeniable.

It need not, in fact, take much hunting to push such large-bodied, slow-reproducing species away from an equilibrium balance of births and deaths. Dr Steven Mithen of Reading University has calculated, for instance, that an expanding population of Palaeoindian colonists hunting mammoths at a rate of just one animal per hunter per year, with a random killing pattern cutting across all age and sex classes, could have driven the mammoths of North America to extinction in less than a millennium.

What is more, recent radiocarbon dates on bone collagen show that mammoths survived in a unique refuge on Wrangel Island in the Arctic Ocean off north-east Siberia until 2000BC or later. By implication, the climatic changes associated with the post-Ice Age warming are not sufficient to account for their extirpation from the mainland of America and Eurasia thousands of years earlier. That's as close as we're likely to get to proof that humans were responsible. Gee, someone ought to tell these paleontologists that early man didn't eat a lot of meat. They ate egg whites and fruit and flaxseed and salmon.

"Sunshine 'Keeps the Elderly Fit and Healthy'Wednesday, May 02, 2007Elderly individuals in the UK should use this week's good weather to top up their vitamin D supplies, if new research is to be believed.

Scientists from Wake Forest University School of Medicine have claimed that older adults who do not get enough vitamin D are at risk of poor physical performance and even disability.

A worrying 25 per cent of those aged 60 or older have low vitamin D levels, the researchers claim. While a subtly altered diet can address this problem to some extent, exposure to sunlight is seen as the only real way to tackle the deficiency.

Vitamin D is produced naturally when human skin is exposed to the sun's ultraviolet rays but, as a result of modern lifestyles, very few people are actually able to enjoy this luxury. Many have also been put off by warnings about the risks of skin cancer - understandable given the rising prominence of this condition in recent years."

"Milk in new possible acne linkWednesday, May 09, 2007New research has suggested that there may be a link between drinking milk and bad skin and acne in teenagers.

Scientists from the Harvard School of Public Health found that teenagers who drank a pint or more of milk a day were 50 per cent more likely to develop spots or pimples than those who drank no milk at all.

And interestingly, skimmed milk was found to be the worst offender, with scientists thinking that the processing of this low-fat version may add to the hormonal content of milk, which has now been linked to increases in acne development.

The research has sparked debate among scientific circles with some experts claiming that acne is fully reliant on genetic factors."

Milk is another unnatural food. Go to www.paleodiet.com and get the real scoop!

Sunbathing may support healthy bonesTuesday, May 08, 2007Scientists still argue that sunbathing is a dangerous pastime but a new report indicates that gentle exposure to the sun's rays can be a very positive thing in maintaining healthy bones.

In a study of over-60s, researchers from Wake Forest University School of Medicine found that physical performance and grip strength were both about five to ten per cent lower in those with low levels of vitamin D. Both are qualities that can be central to quality of life.

And previous research projects in recent years have suggested that vitamin D is hugely important not only for bones but also in the fight against diabetes, cancer, colds and tuberculosis, leading to calls for further investigation about what might constitute healthy levels of exposure to the sun to ensure suitable vitamin D uptake.

"Higher amounts of vitamin D may be needed for the preservation of muscle strength and physical function as well as other conditions such as cancer prevention," commented lead researcher Dr Denise Houston.

A 2005 study conducted at the University of California found that high doses of vitamin D can reduce the risk of developing certain cancers by around 50 per cent. This one is a huge turnaround. Turns out we need sun (but NOT SUNBURN) to get lots of Vitamin D. We're deficient because GRAIN has PHYTIC ACID that leeches all the Vitamin D out of our body and gives us cancer and destroys our bones. Stop eating BREAD!

A leading independent health organisation has recommended that doctors make a better diet, including consumption of more oily fish and omega-3 fatty acids, part of their recommendation for patients who have suffered heart attacks.

The National Institute for Health and Clinical Excellence (NICE) has said that healthy lifestyle recommendations should go alongside prescribed drugs in efforts to help prevent repeat attacks.

NICE has updated guidelines it last set out in 2001, and now recommends two to four portions of fish a week for heart patients. If that figure cannot be met, then the guidelines suggest that the fish can be replaced with daily omega-3 supplements of at least 1g.

Dr Gill Leng, NICE implementation systems director, commented that the new framework should help ensure a "coherent and consistent approach amongst clinicians of all disciplines and places of practice".

"Its overall aim is to provide the growing number of people who now survive a heart attack with the good quality systematic care that is essential to improving long term outcomes and quality of life," added Dr Leng.

As part of a more Mediterranean-style diet, other foods that should be incorporated into the diet of past heart attack sufferers include bread, fruit and vegetables - while meat intake should be reduced.

What a crock of shit! Eat more Omega3. Where does Omega3 come from? Meat. Oh, but eat less meat. !!!?? Eat grassfed beef and game meats and you'll have all the Omega3 you need, with little saturated fat. Oh, and the fish, if it's farm raised is fed GRAIN! That means no omega3! So while I'm eating a grassfed steak filled with Omega3, some jerk is eating a farm raised salmon with none at all and smuggly smirking to himself. What an asshole!

* Reduce inflammation throughout your body * Keep your blood from clotting excessively * Maintain the fluidity of your cell membranes * lower the amount of lipids (fats such as cholesterol and triglycerides) circulating in the bloodstream * decrease platelet aggregation, preventing excessive blood clotting * inhibit thickening of the arteries by decreasing endothelial cells' production of a platelet-derived growth factor (the lining of the arteries is composed of endothelial cells) * increase the activity of another chemical derived from endothelial cells (endothelium-derived nitric oxide), which causes arteries to relax and dilate * reduce the production of messenger chemicals called cytokines, which are involved in the inflammatory response associated with atherosclerosis * reduce the risk of becoming obese and improve the body's ability to respond to insulin by stimulating the secretion of leptin, a hormone that helps regulate food intake, body weight and metabolism, and is expressed primarily by adipocytes (fat cells) * help prevent cancer cell growth

What conditions or symptoms indicate a need for more high-omega-3 foods?

Salmon, flax seeds and walnuts are excellent food sources of omega 3 fatty acids. I love how all these sites first tell you how important omega3 is, and then when it comes to the "where to get it" section, they fall flat. Let's face it, a nutrient this vital to human health in every single way, would probably not be hard for humans to find, right? Or else why would humans have evolved to need it so badly? Our brains are MADE OUT OF OMEGA3! So the success of our whole species is predicated on our ability to get fish from the deepest depth of the ocean? How did cavemen do this? How do people in arid or mountain or inland environments get omega3? From salmon? From flaxseed? Have you even seen flaxseed in your entire life? I haven't! Spend a few weeks hiking through the Smoky mountains, and tell me where you find flaxseed and salmon? You don't! Here's where you get omega3- FROM MEAT!!! But here's the catch, when we make meat now, we feed the animals cereal grains, which are an unnatural food for us and for the animals. Grains knock the omega3's right out of our meat. So instead of eating grassfed beef like our ancestors did, and like the do in Europe, or ordering it from a independent American rancher, we go off searching for flaxseed, or some possibly poorly preserved gel cap. Eat grassfed beef! A quick google search will help you locate dozens of suppliers.

Here's yet another bit of research connecting fat to fructose-laden beverages A study recently published in Hepatology shows that fructose-laden water (10% wt/vol) decreases liver fat breakdown and causes lipid accumulation in rats.

This change wasnt observed in glucose-fed rats. The rats that drank liquid fructose, unlike those getting glucose, had extra leptin in their blood. However, their livers did not behave as expected given the high levels of leptin, a hormone that generally accelerates fat oxidation in the liver and reduces its synthesis.

The researchers concluded that the fructose-caused lipid accumulation and fatty liver was caused by resistance to the extra leptin. The resistance to leptin decreased the action of a specific receptor (PPAR-alpha), which controls fatty acid oxidation. The researchers noted that because PPAR-alpha activity is lower in humans than in rats, liquid fructose ingestion could cause even worse effects in humans.

Liquid fructose can be found in fruit juice and in any drink with high fructose corn syrup. Non fluid sources are also bad, but the liquid variety seems to be worse because it is absorbed so quickly.

"Swedish researchers say that children with celiac disease are at increased risk of developing type 1.

“Earlier studies suggest that children with type 1 diabetes are more likely to have a subsequent diagnosis of celiac disease,” write the researchers. “However, research is sparse on the risk of subsequent type 1 diabetes in individuals with celiac disease.”"

Wednesday, May 30, 2007

Brain-derived neurotrophic factor (BDNF) is one of a family of neurotrophic factors that participates in neuronal transmission, modulation and plasticity. Previous studies using animals have demonstrated that acute and chronic exercise leads to increases in BDNF in various brain regions. PURPOSE:: To determine the effects of acute exercise on serum BDNF levels in humans, and to determine the relationship between exercise intensity and BDNF responses. Additionally, the relationship between changes in BDNF and cognitive function was examined. METHODS:: Fifteen subjects (25.4 +/- 1.01 yr; 11 male, 4 female) performed a graded exercise test (GXT) for the determination of V O2max and ventilatory threshold (VTh) on a cycle ergometer. On separate days, two subsequent 30-min endurance rides were performed at 20% below the VTh (VTh - 20) and at 10% above the VTh (VTh + 10). Serum BDNF and cognitive function were determined before and after the GXT and endurance rides with an enzyme-linked immunosorbent assay (ELISA) and the Stroop tests, respectively. RESULTS:: The mean V O2max was 2805.8 +/- 164.3 mL.min (104.2 +/- 7.0% pred). BDNF values (pg.mL) increased from baseline (P < 0.05) after exercise at the VTh + 10 (13%) and the GXT (30%). There was no significant change in BDNF from baseline after the VTh - 20. Changes in BDNF did not correlate with V O2max during the GXT, but they did correlate with changes in lactate (r = 0.57; P < 0.05). Cognitive function scores improved after all exercise conditions, but they did not correlate with BDNF changes. CONCLUSION:: BDNF levels in humans are significantly elevated in response to exercise, and the magnitude of increase is exercise intensity dependent. Given that BDNF can transit the blood-brain barrier in both directions, the intensity-dependent findings may aid in designing exercise prescriptions for maintaining or improving neurological health.

See that? Only changes in lactate correspond to changes in BDNF. Score one more for high intensity exercise.

Department of Neurology, University of Muenster, Muenster, Germany. bwinter@uni-muenster.de

Regular physical exercise improves cognitive functions and lowers the risk for age-related cognitive decline. Since little is known about the nature and the timing of the underlying mechanisms, we probed whether exercise also has immediate beneficial effects on cognition. Learning performance was assessed directly after high impact anaerobic sprints, low impact aerobic running, or a period of rest in 27 healthy subjects in a randomized cross-over design. Dependent variables comprised learning speed as well as immediate (1 week) and long-term (>8 months) overall success in acquiring a novel vocabulary. Peripheral levels of brain-derived neurotrophic factor (BDNF) and catecholamines (dopamine, epinephrine, norepinephrine) were assessed prior to and after the interventions as well as after learning. We found that vocabulary learning was 20 percent faster after intense physical exercise as compared to the other two conditions. This condition also elicited the strongest increases in BDNF and catecholamine levels. More sustained BDNF levels during learning after intense exercise were related to better short-term learning success, whereas absolute dopamine and epinephrine levels were related to better intermediate (dopamine) and long-term (epinephrine) retentions of the novel vocabulary. Thus, BDNF and two of the catecholamines seem to be mediators by which physical exercise improves learning.

eMedicine - Dopamine-Responsive Dystonia : Article by N K Nikhar, MD: "The activity of these dopaminergic neurons also has circadian variation. Dopamine production increases through the night with each cycle of rapid eye movement (REM) sleep. The activity at the nigrostriatal terminals is therefore maximal in the early morning; nocturnal variation is more marked in young children and decreases with age. Dopamine activity in nigrostriatal terminals, which already is reduced in patients with DRD, declines further during the course of the day (as well as with increasing age), exacerbating symptoms toward evening and with increasing age."Very interesting. I know that dopamine deficiency is implicated in ADD, and ADD'ers have trouble sleeping. Less sleep could mean less dopamine in the brain.

Although the evidence is growing, they also said there is not yet proof that depression causes diabetes, and there are no definitive explanations of what underlies the connection. But scientists are turning up some clues.

A study at the Joslin Diabetes Center in Boston, published in the journal Diabetes in February, found differences in the brains of people with and without Type 1 diabetes. The brains of diabetics were less dense and less responsive in an area of the prefrontal cortex that helps control emotions and is believed to contribute to depression, said Dr. Alan Jacobson, director of behavioral and mental health research at the Joslin.

Future research is planned to help explain how these changes affect behavior and whether they get worse over time.

Other scientists are looking at the stress hormone cortisol, which builds up in many depressives. Cortisol decreases the body's production of insulin and reduces sensitivity to insulin's effects, which are key characteristics of diabetes. Without enough insulin, the body can't use food to fuel activity.

"That could be the direct link," said Pat Lustman, a professor of psychiatry at Washington University in St. Louis, Missouri. Lustman is testing whether using diet and exercise or drugs to improve insulin sensitivity will boost the effect of antidepressants. Already, other research suggests that easing depression improves diabetics' control of their blood sugar, possibly by improving their body's ability to cope and certainly by increasing their willingness to work at it.

One study, presented in June at the American Diabetes Association meeting, suggested that antidepressants themselves might be part of the connection between depression and diabetes.

[...]

The researchers can't explain the puzzling results. But Richard Rubin, an associate professor at the Johns Hopkins University School of Medicine in Baltimore, who led the study, urged patients not to give up on antidepressants, since the study did not prove that the drugs caused diabetes.

Another part of the puzzle might be disruptions of the immune system that cause inflammation. Both Type 2 diabetes and depression are marked by increased cytokines, immune system proteins that carry messages to the hypothalamus, a part of the brain that helps regulate both mood and blood sugar levels. Researchers are testing treatments that reduce inflammation.

The Dutch group studying depression and diabetes is pursuing a related avenue - that omega-3 fatty acids are a crucial link. These substances, which occur in some fish and plant oils, help brain cells communicate and help reduce inflammation. Low levels of omega-3 fatty acids are linked to depression and may reduce the body's ability to control blood sugar.

The group is testing whether doses of omega-3 fatty acids can both improve mood and reduce insulin resistance in diabetics who are depressed.Depression and Diabetes go in hand. Some say that diabetes just sucks and makes people sad. Others say that depression could cause diabetes, by increasing levels of the stress hormone cortisol. Research is ongoing, but I wouldn't be surprised if there is a psiological connection between the two. Mind and body are connected in many different ways. Once again there's an inflammation/omega3 angle to this story.

Here is the question: Why do some addicts relapse even when they sincerely claim that they do not like the substance to which they are addicted? Here is the Berridge and Robinson answer. Liking something is a hedonic process and is associated with its own neural substrate. Liking may explain why addicts initially take and persist in taking drugs (for the pleasure this produces, and to avoid the displeasure of withdrawal). Addicts, however, may re-take drugs after a period of refraining, long after the displeasures associated with withdrawal are past, and for no anticipated pleasure. This is because the neural systems that are sensitized to drug taking are connected with wanting or desiring. These are dopamine systems and they are not the same substrates as those for liking. Addicts may want drugs or be motivated to take them even if they rightly believe that they don't like them, and therein are both unawares of wanting them and unprepared to inhibit the impulse to seek them.

One clinical lesson of the distinction is that persons should continue to exercise watchful restraint over stimuli for addictive behavior even if, or perhaps just because, they feel no need to restrain themselves since the drug is no longer liked. So says the theory. That's a potentially potent idea, I believe, for, if sound, it applies to a lot of human behavior that is imprudent and disordered even if not specifically addictive. Consider, for example, obsessive-compulsive behavior, whose subject may claim that they receive no relief at all from washing their hands, and dislike the chore, but persist in the behavior and become anxious when stymied. West utilizes the idea in PRIME. Cigarette smoking may feel so disliked that an individual feels inhibited from lighting up. But beware. The impulse to smoke and motivation to renew one's engagement with cigarettes may abide.

In addition to his own theory of addiction and assessments of other theories, there is a lot of just plain useful information about addiction that West shares in this book. Did you know that it is rare for efforts to overcome addiction to be successful the first time? Did you know that adults who engage in one type of addictive behavior often (albeit not universally) engage in others?

This is from a book review. I am intrigued by the difference between liking and wanting, with dopamine controlling the "wanting" part. So you could like something, but if dopamine is lacking, you don't have the drive to seek it out. Addicts have the reverse problem, where dopamine has entrained itself to seek the addiction object, despite the dislike the subject ma feel. I wonder what causes the liking part? Serotonin perhaps? Or perhaps Dopamine, but in a different area of the brain?

Last week, the Lebanese army attacked a squalid Palestinian refugee camp that’s become infested with Islamist suicide terrorists and guerilla fighters. On May 20, government troops surrounded the camp, with tanks and artillery pieces shelling it at close range. Army snipers gunned down anything that moved. At least 18 civilians were killed, and dozens more injured. Water and electricity were cut off. By week’s end, much of the camp had been turned into deserted rubble. Thousands of terrified residents fleeing the camp reported harrowing stories of famished, parched families trapped in their basements.

How did the rest of the world react? The Arab League quickly condemned “the criminal and terrorist acts carried out by the terrorist group known as Fatah al-Islam,” and vowed to “give its full support to the efforts of the army and the Lebanese government.” EU foreign policy chief Javier Solana also condemned Fatah al-Islam, and declared Europe’s “support” for Lebanon. And the UN Security Council called the actions of Fatah al-Islam “an unacceptable attack” on Lebanon’s sovereignty. As for the Western media, most outlets ignored the story following the first flurry of news reports.

At this point, please indulge me by re-reading the first paragraph of this column — except this time, substitute the world “Israeli” for “Lebanese” in the first sentence. Let’s imagine what the world’s reaction would be if the ongoing siege were taking place in Gaza or the West Bank instead of the Nahr al Bared refugee camp on the outskirts of Tripoli, Lebanon.

First of all, a flood of foreign journalists would descend on the camp to document Israel’s cruelty and barbarism, and the story would remain front page news to this day. Al-Jazeera would be a 24/7 montage of grieving mothers swearing revenge on the Zionist butchers, and rumours would swirl of mass graves and poison gas. The Arab League, EU and United Nations would condemn Israeli aggression — as would the editorial board of The New York Times. The Independent would dispatch Robert Fisk to embed with Fatah al-Islam. And the newspaper’s cartoonist, Dave Brown, would produce another award-winning rendition of his signature theme: Jews eating Palestinian babies.

Actually, we don’t need to speculate: What I have just written is exactly what happened when the Israeli army invaded the Jenin refugee camp to root out terrorists in April, 2002, a battle that was similar in scale to this month’s siege at Nahr al Bared. (At Jenin, 52 refugee camp residents were killed — most of them gunmen, according to Human Rights Watch. At Nahr al Bared, the figure is 45 and climbing.) The main difference between the two sieges is that Israel’s army put its troops at far greater risk by invading Jenin with infantry — whereas the less humane Lebanese army has simply pummelled Nahr al Bared with explosives from a distance. Jews apparently care a lot more about saving Palestinian civilians than do Lebanese soldiers.

For years, we have been told that Palestinian suffering and “humiliation” is at the root of the Middle East conflict, as well as the Western-Muslim clash of civilizations more generally. This is nonsense: The 200,000-plus Palestinian refugees who live in Lebanese camps are treated worse than dogs — with no access to decent schools or good jobs — and no one in the Arab world cares a whit.

Tuesday, May 29, 2007

"CARACAS, Venezuela (AP) - President Hugo Chavez defended his decision not to renew the license of a popular opposition-aligned television network on Tuesday and warned he might crack down on another critical TV station, accusing it of trying to incite attempts on his life.

Chavez said his refusal to renew the license of Radio Caracas Television, which went off the air at midnight Sunday, is 'a sovereign, legitimate decision in which there is no argument.'

He said the remaining opposition-sided channel Globovision had encouraged attempts on his life and warned that if it wants 'to continue calling for disobedience, inciting assassination ... I'm going to warn them before the nation... I recommend they take a tranquilizer, that they slow down, because if not, I'm going to slow them down.'

Chavez did not elaborate, but also warned that radio stations should not be inciting violence by 'manipulating feelings' among the populace.

Thousands of Venezuelans—both Chavez supporters and opponents—staged separate marches in Caracas on Tuesday. The Chavez opponents chanted 'freedom!' while government supporters said they were in the streets to reject an opposition attempt to stir up violence."

Chavez continues to take away freedom, to make a "worker's utopia". Yeah, good luck with that.

Iran, the United States and Potential Iraq Deal-SpoilersBy Reva Bhalla

After 27 years of frozen relations, the United States and Iran held their first high-level direct talks in Baghdad on May 28 to negotiate a plan on how to stabilize Iraq. U.S. Ambassador to Iraq Ryan Crocker and his Iranian counterpart, Hassan Kazemi-Qomi, traded accusations about who was the bigger destabilizing force in Iraq. But by the end of the four-hour meeting, both described the negotiations as a positive first step in bringing the two sides together to stabilize Iraq. Kazemi-Qomi even said there probably would be a follow-up meeting within a month if he gets the OK from Tehran.

Iran and the United States evidently have come a long way since the spring of 2003, when Washington double-crossed Tehran on the two countries' original understanding that a pro-Iranian, Shiite-dominated Iraq would be allowed to emerge in exchange for Iran's help in effecting regime change in Baghdad. When the United States removed two hostile Sunni regimes from Iran's border -- the Taliban in Afghanistan and Saddam Hussein in Iraq -- the Iranians knew they had to check the United States on the regional chessboard so Washington understood any U.S. exit strategy from Iraq would have to come through Tehran. Only then, Tehran reasoned, could Iran use Iraq as a launchpad to extend Iranian influence in the Arab world.

Feeling a deep sense of betrayal, the Iranian government carried out a variety of deadly maneuvers that ultimately convinced Washington that neither the Iranians nor the Americans were going to succeed in gluing Iraq back together on their own. The negotiations are still marred by mutual distrust, but after four years of explosive negotiating tactics, Iran and the United States have reached a point at which both sides have acknowledged they cannot afford to avoid each other if they want to avoid their worst-case scenarios in Iraq.

As the negotiations grow in intensity, so does the noise. The lead-up to the May 28 talks was punctuated by a series of interesting jabs as each side sought leverage against the other. While the United States sent nine warships with 17,000 troops into the Persian Gulf (which the U.S. military deliberately referred to as the Arabian Gulf in the official press release on the naval exercises) and stepped up threats of broadening sanctions against Tehran due to the latter's nuclear activities, Iran continued broadcasting its atomic advances and announced it had uncovered Western-run spy rings inside the Islamic republic. The United States is still holding onto five Iranian officials arrested in the northern Iraqi city of Arbil in January as bargaining chips in talks with Iran. Iran has responded with a series of arrests of Iranian-Americans affiliated with think tanks on allegations they are dissidents working to topple the clerical regime. These belligerent tactics are all part of the game, and will flare up even further as the negotiations grow more serious.

The Meat of the Matter

It now becomes all the more critical to cut to the meat of these talks: the negotiating terms put forth by Washington and Tehran over how each plans to fix Iraq.

Iran handed over a proposal to Crocker during a brief encounter at the May 5-6 Sharm el-Sheikh summit in Egypt, but also chose to unofficially publicize its terms for Iraq through the Saudi-owned, British-based daily Al Hayat. The Iranian Foreign Ministry likely chose Al Hayat, a major Arab news outlet, to make a back-channel broadcast of what concessions it is prepared to make to allay Sunni concerns in the region.

In sum, this Iranian proposal called for a non-rushed withdrawal and relocation of U.S. troops to bases inside Iraq, a rejection of all attempts to partition Iraq, a commitment by the Sunni bloc to root out the jihadists and acknowledgement by Washington that the Iranian nuclear file cannot be uncoupled from the Iraq negotiations. In return, Iran would rein in the armed Shiite militias, revise the de-Baathification law and Iraqi Constitution to double Sunni political representation, create a policy to allow for the fair distribution of oil revenues (particularly to the Sunnis) and use its regional influence to quell crises in areas such as Lebanon, Syria and the Palestinian territories.

The terms put forth by the Iranians are so close to the U.S. position on Iraq that, with little exception, they could have been printed on State Department stationary and no one would have noticed the difference. If these are the terms Washington and Tehran are in fact discussing, then we are witnessing an extraordinary turn in the Iraq war in which the U.S. and Iranian blueprints for Iraq are finally aligning. It does not surprise us, then, that Crocker said after his meeting in Baghdad that the Iranian position "was very close to our own" at the level of policy and principle.

The Spoilers

The prospect of Washington and Tehran warming up to each other, and of the United States potentially regaining its military bandwidth in the not-too-distant future, is enough to put a number of serious actors into a frenzy. With the exception of the jihadists, most of the actors in question see an Iranian-U.S. accommodation over Iraq as inevitable, and have little choice but to strive to shape what would otherwise be an imposed reality in the coming months -- leaving substantial room for error in these negotiations. The Iraqi Sunnis and Arab states, in particular, will not necessarily sabotage the talks, but they will be working to secure Sunni interests and contain the extent to which Iran emerges as the primary beneficiary of any deal it works out with the United States over Iraq.

Jihadists

Within Iraq, the transnational jihadists have the most immediate concerns. A political settlement in Baghdad inevitably would involve a concerted effort by Iraq's Shia and mainstream Sunnis to uproot the jihadists and deprive them of the chaotic security conditions needed for their operations. The apex leadership of al Qaeda hiding out along the Pakistan-Afghanistan border is also betting on continued bedlam in Iraq to keep the transnational jihadist movement alive, and will not be happy to see U.S. forces beefed up in the South Asia theater once a deal is sealed in Iraq. Violence aimed at heightening sectarian tensions to derail the negotiations -- particularly attacks aimed at inflaming the Shia -- will escalate substantially over the next few weeks and months in Iraq. High-value political targets also likely will be targeted for assassination in an effort to disrupt the leadership structure of the respective factions.

Iraqi Shia

The Iranians face a daunting task in whipping Iraq's Shiite bloc into shape to follow through with Tehran's commitment to quell sectarian attacks and consolidate Shiite political power in Iraq for the first time in the country's history. Factionalism is already hardwired into the structure of the Iraqi Shiite community, whose loyalties are spread among the three largest political groups -- the (newly named) Iraqi Islamic Supreme Council, Hizb al-Dawah and the al-Sadrite bloc, as well as a number of smaller Shiite groups in southern Iraq, such as the Fadhila party. The intra-Shiite rivalries within and between these groups are enough to give anyone a headache, but Iran is well aware that violence and a good deal of oil money will be needed to bring the Iraqi Shia in line and make these negotiations work. Though the main political groups are more comfortable with the idea of working with Iran, Tehran has to play its cards carefully to ensure it does not trigger nationalist Arab sentiment among the Shiite actors, who already are deeply suspicious of Iran's intentions and have the arms and access to Iraq's southern oil fields to use as tools for stirring up trouble.

Iraqi Sunnis

Though not nearly as fractured as the Iraqi Shia, the Sunni landscape in Iraq has plenty of cracks of its own to make these negotiations troublesome. The Sunni factions in play include:

The existing political blocs, divided between the Islamist Iraqi Accord Front and the secular-leaning Iraqi National Dialogue Front;

The tribal groups, such as Anbar Salvation Council, that are actively fighting transnational jihadists to get a seat at the negotiating table;

The Sunni religious establishment, led by the hard-line Association of Muslim Scholars of Iraq that has close links with the insurgent groups and has become increasingly anti-Iranian in recent weeks;

The Sunni nationalist insurgents, who are looking for an acceptable opening into the political process, but remain distrustful of Shiite intentions.

The Iraqi Sunnis know they have to drive a hard bargain in these talks to ensure that Iraq's Sunnis are well-integrated in the state political and security apparatus to counter the Shiite majority. And they will continue to rely on explosives during the talks to make sure their demands are heard. Competing factions within the Sunni bloc and resistance from their former jihadist allies will only further complicate these negotiations, but unlike the jihadists, these Sunni groups are not opposed in principle to a deal that includes the Iranians -- they actually want negotiations.

Iraqi Kurds

By the looks of the Iranian proposal, the Kurds have plenty to worry about. Expanding Sunni political representation and changing the constitution to allow for a more "fair" distribution of oil resources leaves the Kurdish bloc in an all-too-familiar scenario in which Kurdish interests will be sacrificed by the United States to protect the interests of Iraq's neighbors.

Thus far, the Kurds have used the distraction of Sunni-Shiite bloodletting farther south to consolidate power between the two main rival Kurdish blocs (an extremely rare occurrence) and push forward with Kurdish autonomous demands to open Iraq's northern oil fields to foreign business. Once Iraq's Shiite and Sunni blocs reach some level of a political understanding in Baghdad, their attention will soon turn to their common adversary in the north, leaving the Kurds to face familiar moves by the Iraqi government to suppress Kurdish autonomy. The Kurds will need to drive a hard bargain by pushing through a Kirkuk referendum by year's end and resisting radical changes to the constitution and pending hydrocarbons legislation that threaten to put Iraq's undeveloped fields in the north under state control. The biggest threats the Kurds could make to a U.S.-Iranian deal over Iraq would involve withdrawing Kurdish support for U.S. forces or threatening to pull out of the government. But in the end, a compromise looks inevitable simply because the Kurds have nowhere else to turn.

Ultraconservatives in Washington and Tehran

There are ultraconservative factions in both Tehran and Washington that are not nearly as enthused about a U.S.-Iran rapprochement, and could use their influence to complicate the negotiations. Rumor has it that in Iran there are major disagreements brewing between the president and other senior Iranian officials, particularly on foreign policy matters. There are also growing indications that the apex of the clerical establishment is making moves to sideline Iranian President Mahmoud Ahmadinejad and weaken the influence of his ultraconservative faction as a preventative measure to ensure progress in these talks. Though Iranian Supreme Leader Ayatollah Ali Khamenei has thus far managed the deep divisions within the Iranian establishment between the ultraconservative and pragmatic conservative factions, his ability to contain these divisions is held hostage by his failing health.

Meanwhile, hard-line elements in Washington are actively spreading information in an allegedly covert campaign signed off on by U.S. President George W. Bush to topple the clerical regime. These actors are more interested in effecting a policy of regime change rather than in a rapprochement with Iran, and they view the negotiations as little more than a smoke screen for a covert campaign to rid the Islamic republic of its ruling ayatollahs. These rumors threaten to fuel even more distrust between the two sides while the negotiations are in full swing, especially as Iran's greatest fear is that it will end up being backstabbed all over again once Washington recovers from Iraq and has enough bandwidth to entertain military options.

Sunni Regional Powers

Saudi Arabia and the Gulf Arab states are extraordinarily nervous about the idea of having the United States and Iran conduct exclusive meetings over a matter that directly concerns their national security interests. As the leader of the Sunni Arabs, the Saudis believe they have every right to be part of the formal negotiating process, but they also see the inevitability of the United States and Iran working toward an Iraq settlement. With the most at stake, the Saudi government normally would be screeching in protest during these U.S.-Iranian bilateral meetings, but instead it is keeping quiet. For now, the Saudis have to rely on the United States to ensure their demands for Sunni representation and Iranian containment are heard.

Meanwhile, the Iranians evidently are working to allay Sunni Arab fears by publicizing Tehran's Iraq proposal (with considerable concessions to Iraq's Sunnis) in the mainstream Arab press and stepping up diplomatic engagements with Iran's Sunni neighbors in the Gulf. But the more the Iranians speak of arming and training the Iraqi army, the more the Saudis have to worry about. The House of Saud does not want to be looking at a scenario down the road in which U.S. troops have withdrawn from Iraq while Iran uses its militant proxies there to create an excuse to intervene militarily, putting Iranian troops within sight of Saudi Arabia's oil- and Shiite-rich Eastern province. The Saudis are also not looking forward to the day when war-hardened Saudi jihadist veterans in Iraq return home to wage attacks in the kingdom. Though the Saudis might see an Iran-U.S. deal as inevitable, they will keep their ties to the full spectrum of Sunni militants to use as their main deal-breaker should an Iraq settlement fail to address their interests.

Syria

Syrian President Bashar al Assad also probably is lying awake at night over these U.S.-Iran talks. The Alawite-Baathist regime in Syria loved the idea of its allies in Tehran expanding Shiite influence while the United States remained far too militarily occupied in Iraq to bother with Syria. The insurgency in Iraq also provided Syria with a vital pressure release valve for Sunni militants in the country. Like Riyadh, the regime in Damascus does not want to see jihadists returning home from Iraq to carry out attacks on native soil.

Despite these concerns, the Syrians are hoping their alliance with Tehran will pay off and result in serious recognition and security assurances from the United States. For this to happen, Syria has to prove it is an integral piece of this Iraq deal by showing it possesses the ability to clamp down on insurgent traffic (by funneling jihadists into Lebanon for now). While Syria offers limited cooperation over Iraq to show its powers, the al Assad regime will become further emboldened to secure its interests in Lebanon, where Syria's priorities are rooted.

Russia

But the player with perhaps the most to lose is not even located in the Middle East. That player is Russia. At first glance, Russia is an odd party to even be involved in the Iraqi imbroglio. It has no troops in country and, no matter what happens to Iraq in the long run, Baghdad has no impact on anything Russian. Certainly Moscow was friendly with the previous government, but not to the degree that Saddam Hussein's fall appreciably impacted Russian political or economic interests.

Russia does, however, have two horses in this race.

The first relates to the Iranian nuclear program, which lists the Russian-built Bushehr power plant as its crown jewel. Despite Iranian protestations to the contrary, Tehran's nuclear program is largely a result of Russian technology sharing. And, should the Russians walk away, the Iranian program will have suffered a monumental setback. Similarly, so long as Russia has not finished the reactor at Bushehr, the West cannot ignore Moscow's ability to function as an interlocutor in Tehran. So long as the facility is "under construction," Russia has leverage over both parties. As soon as Russia's technicians finish, however, that leverage evaporates.

Second, and far more important: So long as the bulk of the United States' and Iran's political and military attention is absorbed in Iraq, neither has any bandwidth to deal with other issues. Iran has deep and lasting interests in Azerbaijan and Turkmenistan -- states of critical interest to Moscow -- yet Iran's preoccupation with Iraq has prevented Tehran from capitalizing on recent opportunities. Similarly, the United States has faced no foe more challenging than the Soviet Union and its Russian successor. In that vein, there is no country more desirous of challenging Russia's ongoing efforts to rewire European security arrangements in its own favor than the United States. But that requires a Washington not consumed by the black hole Iraq has become.

A Rough Road Ahead

It took four years of heavy-handed negotiating tactics to bring U.S.-Iranian dealings over Iraq out of the back channels and into the public view.

That was half the battle.

This is from Stratfor's email update service. STRATFOR ROCKS! I encourage you to visit their site and sign up for their analysis. They're really like a private CIA. It's expensive to get their full updates, but get their free email updates!

But which genes are involved? One line of evidence leads to serotonin, which has numerous functions in the nervous system including an influence on mood, memory and learning. Irregularities in the expression or control of serotonin have been linked to depression, anxiety and a variety of other disorders. Drugs such as Prozac™ which affect serotonin are are now widely used in medicine.

In 1996, geneticist Dean Hamer of the National Institutes of Health and his colleagues reported that they had found an association between the serotonin transporter gene and neuroticism, a complex of behaviors that includes depression, low self-confidence, and shyness around strangers. Hamer reported in Science that adult volunteers who rated high on the scale of neuroticism tend to have a short version of the serotonin transporter promoter, a stretch of DNA that controls how much of the serotonin transporter gets made. Adults who ranked low in neuroticism tended to have a long version of the promoter.

Both the long and short copies of the gene are functioning, says Hamer. However, the short version appears to result in less of the serotonin transporter, and thus less serotonin activity. Hamer called it the "anxiety gene." Meanwhile, other studies suggest that another gene, DRD4, may also play a role in traits such as shyness and anxiety. The DRD4 gene codes for a protein that binds dopamine, another chemical messenger that has powerful effects in the brain. Again, the DRD4 gene comes in two forms: a long and a short version.

In a study reported in a recent issue of Molecular Psychiatry, behavioral scientist Judith Auerbach, of Ben-Gurion University, Beer Sheva, Israel, said that infants with short copies of the DRD4 gene and serotonin transporter promoter are less responsive to stimulation and show more distress during daily routines, compared to infants with different versions of these genes. Auerbach cautions that her findings do not define a gene or genes that predispose infants to future shyness. "That will only be clearer when the infants are older," says Auerbach, who is continuing to study the behavior of these infants as they grow. It is also interesting that a number of studies have linked the longer DRD4 gene to novelty-seeking behavior, just the opposite of being shy.

So there's a gene for ADHD, but not everyone with the gene (allele 10 variant of the VNTR 40 base pair DAT gene) gets ADHD. They studied a bunch of kids and found that kids with the gene AND ADHD had some family stressors. So you need the gene, and environmental stress to develop ADHD. I would imagine that physical stresses, like a mother smoking while pregnant (a risk factor for ADHD) could also have the same effect). Or not getting enough sleep. I finally got a good nights sleep last night and I feel fantastic today! I should sleep 18 hours every day!

Depression and ADHD. They just go together. Problem is, patients and clinicians alike are too little aware of this common combination. That has major consequences.

Here are relevant statistics from one study.* Kessler and his colleagues looked at subjects who, within a year, met diagnostic criteria for clinical depression (major depressive disorder). Of these persons with severe depression, the researchers found that 9.4 % also met criteria for ADHD. That’s almost one in 10.

Conversely, the findings were more marked when the researchers looked at study subjects who initially met criteria for ADHD. Nearly 1 in 5 (18.6%) also met criteria for clinical depression within the previous year.

An estimated 5 -10% 0f patients with the most severe mood disorder, bipolar disorder (manic-depressive illness) also have ADHD.

1. Educate yourself about ADD. Read books, talk to your doctor, therapist, coach, other adults with ADD, join a support group, either in your area or online. The more you understand ADD, the more you will be able to help yourself and work together with medical professionals in determining the best treatment.

2. Use structure in your life. Create lists, write yourself notes, use a tape recorder to record messages to yourself, use an organizer such as a dayplanner or a PDA. The more structure you create in your life, the more you can control the downslide of disorganization.

3. Always break tasks down into small chunks. Large tasks tend to overwhelm the adult with ADHD, breaking them down into small chunks can help you manage the task more easily.

For example, instead of “I’m going to clean the house today” focus one particular aspect, such as “First, I am going to straighten up the living room.” Then set about to complete that part of the task before moving on to the next part.

4. Learn your own patterns and use them to your benefit. If you work best in the afternoon and evening, try to find a job where you would be able to work those hours. If you find yourself sluggish each afternoon, plan your day accordingly to make the most of your own patterns of behavior.

5. Make time for yourself. Find transitional times in between activities. Take a 10 minute stop at a park on your way home from work to unwind and prepare for home life, or set aside a few minutes after the morning rush to get everyone else out of the house to prepare for your day.

6. Prioritize your responsibilities and obligations. Determine what is really important and take care of that before starting something else.

7. Find time to be with people that understand and accept you. If you find that you are in a position where people judge you or make you feel uncomfortable, leave. Create a network of people that you can talk with freely and feel important with.

8. Set deadlines for yourself. Procrastination is a big problem for adults with ADD, setting deadlines can help you to limit procrastination and complete tasks.

9. Exercise on a regular basis. Exercise is a way to increase the chemicals in the brain needed for focus and attention, helps decrease excessive energy and helps calm you down.

10. Accept yourself. Remember that ADHD is a neurological disorder. Although this doesn’t mean that it is an excuse for unacceptable behavior, it can explain certain behaviors.

A cognitive bias is something that our minds commonly do to distort our own view of reality. Here are the 26 most studied and widely accepted cognitive biases.Bandwagon effect - the tendency to do (or believe) things because many other people do (or believe) the same. Related to groupthink, herd behaviour, and manias. Carl Jung pioneered the idea of the collective unconscious which is considered by Jungian psychologists to be responsible for this cognitive bias.Bias blind spot - the tendency not to compensate for one’s own cognitive biases.Choice-supportive bias - the tendency to remember one’s choices as better than they actually were.Confirmation bias - the tendency to search for or interpret information in a way that confirms one’s preconceptions.Congruence bias - the tendency to test hypotheses exclusively through direct testing.Contrast effect - the enhancement or diminishment of a weight or other measurement when compared with recently observed contrasting object.Déformation professionnelle - the tendency to look at things according to the conventions of one’s own profession, forgetting any broader point of view.Disconfirmation bias - the tendency for people to extend critical scrutiny to information which contradicts their prior beliefs and uncritically accept information that is congruent with their prior beliefs.Endowment effect - the tendency for people to value something more as soon as they own it.Focusing effect - prediction bias occurring when people place too much importance on one aspect of an event; causes error in accurately predicting the utility of a future outcome.Hyperbolic discounting - the tendency for people to have a stronger preference for more immediate payoffs relative to later payoffs, the closer to the present both payoffs are.Illusion of control - the tendency for human beings to believe they can control or at least influence outcomes which they clearly cannot.Impact bias - the tendency for people to overestimate the length or the intensity of the impact of future feeling states.Information bias - the tendency to seek information even when it cannot affect action.Loss aversion - the tendency for people to strongly prefer avoiding losses over acquiring gains (see also sunk cost effects)Neglect of probability - the tendency to completely disregard probability when making a decision under uncertainty.Mere exposure effect - the tendency for people to express undue liking for things merely because they are familiar with them.Omission bias - The tendency to judge harmful actions as worse, or less moral, than equally harmful omissions (inactions).Outcome bias - the tendency to judge a decision by its eventual outcome instead of based on the quality of the decision at the time it was made.Planning fallacy - the tendency to underestimate task-completion times.Post-purchase rationalization - the tendency to persuade oneself through rational argument that a purchase was a good value.Pseudocertainty effect - the tendency to make risk-averse choices if the expected outcome is positive, but make risk-seeking choices to avoid negative outcomes.Selective perception - the tendency for expectations to affect perception.Status quo bias - the tendency for people to like things to stay relatively the same.Von Restorff effect - the tendency for an item that “stands out like a sore thumb” to be more likely to be remembered than other items.Zero-risk bias - preference for reducing a small risk to zero over a greater reduction in a larger risk.

Oh and, by the way, you’ll never be able to truly gauge any of the biases you might be operating under since it’s not possible to accurately observe a system you’re part of. Now, get out there and delude yourself!

Humans hard-wired to be generousA study by government scientists in Washington indicates humans are hard-wired to be unselfish.

"Neuroscientists Jorge Moll and Jordan Grafman of the National Institutes of Health say experiments they conducted have led them to conclude unselfishness is not a matter of morality, The Washington Post reports.

Rather, the two say altruism is something that makes people feel good, lighting up a primitive part of the human brain that usually responds to food or sex."

HAI! This site provides community documentation of the emergent LOLCODE language. It is our hope that the examples can grow in a way that is both internally consistent and suggest a real, feasible computing language.

The best way to start the site is with some examples to give the flavor of the language.

Wow, hello, new users! Stick around, and get comfortable. I’ve only just started the site. I’m blown away by the creativity of the contributions coming into the site and by email, and want to be able to push new keywords into the canon soon. Examples

Explanation: Black spots have been discovered on Mars that are so dark that nothing inside can be seen. Quite possibly, the spots are entrances to deep underground caves capable of protecting Martian life, were it to exist. The unusual hole pictured above was found on the slopes of the giant Martian volcano Arsia Mons. The above image was captured three weeks ago by the HiRISE instrument onboard the Mars Reconnaissance Orbiter currently circling Mars. The holes were originally identified on lower resolution images from the Mars Odyssey spacecraft, The above hole is about the size of a football field and is so deep that it is completely unilluminated by the Sun. Such holes and underground caves might be prime targets for future spacecraft, robots, and even the next generation of human interplanetary explorers."

A response from retired Master Sergeant Gid L. White. After Katie Couric declared that there were no atheists in foxholes on a TV newscast:

Dear Miss Couric,

While there is nothing wrong highlighting in the program the role that religion has played in the American Armed Forces, I find your mindless parading of that silly old aphorism, “there are no Atheists in foxholes,” to be thoughtless and downright offensive to the families of uncountable numbers of atheists, and I include Agnostics, who gave their lives wearing the uniform of the American Armed Forces. Yes, there are, and always have been Atheists, both draftees and volunteers on the battlefield, many of whom bare the scars of war or are ironically buried below white crosses in battlefields throughout the world.

I’m in a position to know. After initially being nominated to WestPoint, I enlisted in the United States Army as a Private in 1964, where I served 21 years on active duty retiring as a Master Sergeant in 1985. As one who is not shy about proclaiming my firm non-belief in any supernatural nonsense, religious or otherwise, I became aware of literally thousands of fellow Atheists in uniform all over the world. Some were overt and public about their beliefs. Some were not. But all were willing to lay down their lives if necessary. Many did.

The military is fully aware of the existence of Atheists in uniform, and in fact makes specific allowances for us in the oath enlistment. In the oath there is a clear choice. We can swear before God, the Great Pumpkin, or whatever, to serve our country. Or we can affirm the oath. There are no bibles or other sacred books used in this oath unlike for some political offices. The only item required to be present is the American Flag. All my reenlistments were affirmed as were hundreds of others I witnessed. Under affirmed oath I personally encountered dozens of soldiers wearing purple hearts bronze stars and at least five silver stars. Among them were Special Forces, Rangers, and Intelligence Officers, Artillerymen, Tank Crewmen, Cooks, Paratroopers, Combat Medics, Truck Drivers, and Infantrymen. There are no atheists in foxholes? I beg to differ.

Preachers may blather on about serving for “God and country,” but as any number of combat studies have proven, that is “pure crap,” to use a traditional military term. Soldiers certainly do enlist for patriotic motives and many of them no doubt have deeply held religious beliefs, but this is not why in the heat of combat they risk their lives. They risk their lives for their fellow soldiers, to not let their comrades down, and to secure the survival of their buddies and themselves by getting the job done as rapidly and brutally as possible.

Broadcasting a feel good puff-piece on religion is all well and good, but perpetuating the nonsense that only religious zealots defend their country is not only offensive but demonstrably wrong. Most Atheists and Agnostics in uniform get stuck with the Army’s famous euphemism of “no religious preference” on their dog tags. But mine simply said “Atheist,” after some initial arguments with my superiors. I am offended by your comments primarily in memory of the silent masses of non believers who did not make it back to object to your treatment of their deeply help beliefs. I believe you and NBC owe them an apology.

The team’s work goes back to the 1990s, when they started using ‘metabolic control analysis’ (see Box) to study glucose metabolism in working rat hearts perfused with glucose, to which ketones or insulin or both have been added [2]. Insulin is a hormone that reduces glucose concentration in the blood, and deficiency of insulin is associated with type I diabetes.

Radioactive glucose was used to keep track of the rate at which glucose disappears and becomes transformed into different metabolites including glycogen (a storage product which is a large polymer of glucose). The results show that no single enzyme controls glucose metabolism. Instead, different enzymes are in control, depending on the prevailing conditions. For example, the heart works better in the presence of either ketones or insulin, but the combination of both ketones and insulin is no better than either alone. In the presence of glucose only, glycogen is broken down. With the addition of ketones, insulin or both, glycogen is synthesised. The concentrations of practically all the metabolites downstream of glucose are changed, many significantly, by the addition of ketones or insulin or both; as are the concentrations of the major energy intermediates, ATP and creatine phosphate.

At the same time, the effciency of the working heart increases by 25% in the presence of either insulin or ketones, and by 36% in the presence of both. The increase in efficiency is accompanied by dramatic changes in key metabolites in energy metabolism (those reactions leading directly to generating ATP in the mitochondria). The most interesting finding is that ketones appear to change the profile of energy metabolism in ways similar to insulin, which the researchers conclude, may have important clinical consequences. It has been shown

previously that increase in blood ketones to levels observed after a 48h fast almost completely reversed the mitochondrial abnormalities associated with insulin deficiency. Moderate increases in circulating ketones, the authors suggest, "should be viewed as a beneficial compensation for insulin deficiency and perhaps also for geriatric patients or others with peroxidative damage to the processes of mitochondrial energy transduction" [4]. Could it be that ketones may also help type I diabetes?

The next obvious step is phase I clinical trial in Alzheimer’s and Parkinson’s patients. The problem is that ketones can’t be taken directly because they are too acidic. A trimer (a molecule that consists of three ketones joined end to end) is neutral, and would be suitable as a food supplement. The bad news for Veech is: no drug company will make the stuff for him, while the institution Veech works for, the NIH, does not even consider his research worth funding in the mad dash for genetic causes of diseases and gene-based drug and interventions.

The good news is that the Navy will be funding the project, so the clinical trial will go ahead after all. Watch this space.

SummaryKetosis, meaning elevation of D-¯-hydroxybutyrate (R-3-hydroxybutyrate) and acetoacetate, has been central to starvingman’s survival by providing nonglucose substrate to hisevolutionarily hypertrophied brain, sparing muscle from destructionfor glucose synthesis. Surprisingly, D-¯-hydroxybutyrate(abbreviated “¯OHB”) may also provide a more ef cient sourceof energy for brain per unit oxygen, supported by the same phenomenonnoted in the isolated working perfused rat heart and insperm. It has also been shown to decrease cell death in two humanneuronal cultures, one a model of Alzheimer’s and the other ofParkinson’s disease. These observations raise the possibility that anumber of neurologic disorders, genetic and acquired, might bene t by ketosis. Other bene cial effects from ¯OHB include an increasedenergy of ATP hydrolysis (1G0 ) and its linked ionic gradients.Thismay be signi cant indrug-resistant epilepsy and in injuryand anoxic states. The ability of ¯OHB to oxidize co-enzyme Q andreduce NADP+ may also be important in decreasing free radicaldamage.

[...]

Fear of KetosisPhysicians have long been taught to fear ketosis; the hallmarkof potentially fatal diabetic ketoacidosis

[...]

Ketosis is the Physiological Response to Fastingin Homo sapiensThis fear of ketosis may be exaggerated. Mild ketosis canhave therapeutic potential in a variety of disparate disease states.Blood ketone bodies reach 5–7 mM in fasting man (2) and areessential to preserve muscle mass from conversion to glucosefor brain consumption. Episodic starvation was a normal stateduring the evolution of the hunter-gatherer. Mild ketosis (2–7 mM) remains today peculiar to man as a species (except insome ruminants, particularly during exuberant lactation or duringtwinning). Man is distinguished from other animals by hislarge brain/body weight ratio and brain’s very high energy requirements.At rest, 20% of oxygen consumption is needed to support the 1.5 kg of brain, which is2% of body weight. It can beargued that since ketone bodies are the only available alternativeto glucose for brain’s energy, ketosis was a critical evolutionarydevelopment to provision man’s hypertrophied brain whilesparing muscle mass (3). The survival bene t is obvious; about2 months for an average weight starving adult compared to acalculated 2–3 weeks were ketone bodies not available.

Ketosis as Treatment for EpilepsyThe ability of brain to use ketone bodies, with one notable exception,the treatment of epilepsy by prolonged fastings, has notbeen utilized therapeutically.

[...]

(description of fasting and zero carb diets to stop seizures in epilepsy)[...]

THE EFFECTS OF KETONE BODY METABOLISMImprovement in Metabolic EfciencyIn the 1940’s it was observed that ¯-hydroxybutyrat e and acetoacetatewere unique among the 16 carbohydrates, lipids, andintermediary metabolites tested on sperm in their ability to decreaseoxygen consumption while increasing mobility (9, 10).The reasons for this apparent increase in metabolic ef ciencyremained a mystery for 50 years. Recently, detailed studies byVeech and colleagues of the metabolism of ketone bodies in theworking perfused rat heart showed that 5 mM ketone bodiesadded to the glucose-containing perfusate resulted in a 25% increasein hydraulic work with a signi cant decrease in oxygenconsumption

[...]

It was thus apparent that the acutemetabolic effects of insulin in working heart could be mimickedby ketone bodies. The implication was that ketosis, whichis the physiological response to insulin deprivation during starvation,was equivalent in metabolic effects to the actions of insulin.By providing an alternative substrate which is transportedinto cells on the monocarboxylate carrier, ketones by-passedthe block in glucose transport caused by lack of insulin, evenstimulating glycogen synthesis (12). Ketones also by-passed theblockade of pyruvate dehydrogenase induced by insulin de -ciency by providing an alternative source of mitochondrial acetylCoA.

[...]

Ketone bodies provide an alternative metabolic fuel which can act duringblockade of glycolysis, as occurs in diabetes or insulin resistance,

[...]

Owen et al. (3) found ow and oxygen consumption to be 45 and 2.96 in 1-monthfastedobese subjects, well below the normal levels reported foradult humans of 57 and 3.6 by McHenry (15). These data suggesta similar increase in metabolic ef ciency in human brainusing ketoacids as the principal source of energy in place ofglucose

[...]

KETOSIS FOR NEURODEGENERATIVEAND OTHER DISEASESAlzheimer’s DiseaseApproximately one  fth of Alzheimer’s disease can be relatedto 5 different genes, all of which lead in one way or another tothe accumulation of amyloid proteins. The remaining cases haveno apparent genetic cause for the increase in amyloid production.The development of metabolic treatments, therefore, offersnovel alternatives to what appears to be a dif cult problem forgenetic manipulations. Several recently published articles givea rationale for the use of mild ketosis as a treatment.

[...]

Parkinson's Disease

[...]

Although the mode of ketone bodyaction has not been thoroughly investigated, it would be reasonableto suppose that they act by decreasing the source ofmitochondrial oxygen radical formation by oxidizing the coenzymeQ couple while at the same time reducing the redoxpotential of the NADP couple which, through glutathione, is the nal detoxi cation step for H2O2. Trials of dopamine therapy incombination with ketone bodies, might be expected to prolongthe useful therapeutic life of dopamine.

d-beta-hydroxybutyrate (DbetaHB) is a predominant member of ketone bodies produced by hepatocytes and, to a lesser extent, by astrocytes. It is an alternative source of energy in the brain when glucose supply is depleted such as during starvation. It has been reported that ketone bodies could protect dopaminergic culture. However, the biological function of DbetaHB in Parkinson disease (PD) is still unclear. In the present work, we investigated the role of DbetaHB in protecting rat pheochromocytoma (PC12) cells from apoptosis induced by 6-Hydroxydopamine (6-OHDA). DbetaHB rescued PC12 cells from apoptotic death induced by 6-OHDA by MTT assay, acridine orange (AO) staining, terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) staining and the activity of caspase-3.

Yeah, this is the kind of stuff I read all the time! Seriously, I find this interesting because here a ketone body is tied to dopamine production and prevention of brain cell death. When your body is low on glucose (starvation or low carb diet), it turns protein from the food you eat (or muscle if you're not eating protein) into glucose for the brain using fat as a fuel source for this process, called gluconeogenesis. Ketone bodies are produced as well, and act as a super fuel for the brain and the body. So there's a tie here between dopamine and ketosis. I guess I keep looking for a link between low carb, diabetes, insulin, dopamine, add, alcholism, etc. I think that many of these systems in the body are redundant and indirect. And all of this is tough for a layman to piece together. But I really think there are ties.

"'The results show dopamine drives us to get what we want, but not avoid what we fear,' said study author Mathias Pessiglione, PhD, who now works at the Salpetriere Hospital in Paris, France.

The findings may provide a better understanding of the side effects of dopamine-related drugs and the disorders they are used to treat, such as Parkinson's disease and schizophrenia. 'This study may explain why dopamine depletion leads to the lack of motivation often described in people with Parkinson's disease,' said Pessiglione, 'and how dopamine replacement therapy can cause compulsive behaviors, such as overeating and gambling addictions, in the same people.'"

A new health scare erupted over soft drinks last night amid evidence they may cause serious cell damage. Research from a British university suggests a common preservative found in drinks such as Fanta and Pepsi Max has the ability to switch off vital parts of DNA.

The problem - more usually associated with ageing and alcohol abuse - can eventually lead to cirrhosis of the liver and degenerative diseases such as Parkinson's.

The findings could have serious consequences for the hundreds of millions of people worldwide who consume fizzy drinks. They will also intensify the controversy about food additives, which have been linked to hyperactivity in children.

Concerns centre on the safety of E211, known as sodium benzoate, a preservative used for decades by the £74bn global carbonated drinks industry. Sodium benzoate derives from benzoic acid. It occurs naturally in berries, but is used in large quantities to prevent mould in soft drinks such as Sprite, Oasis and Dr Pepper. It is also added to pickles and sauces.

Sodium benzoate has already been the subject of concern about cancer because when mixed with the additive vitamin C in soft drinks, it causes benzene, a carcinogenic substance. A Food Standards Agency survey of benzene in drinks last year found high levels in four brands which were removed from sale.

Now, an expert in ageing at Sheffield University, who has been working on sodium benzoate since publishing a research paper in 1999, has decided to speak out about another danger. Professor Peter Piper, a professor of molecular biology and biotechnology, tested the impact of sodium benzoate on living yeast cells in his laboratory. What he found alarmed him: the benzoate was damaging an important area of DNA in the "power station" of cells known as the mitochondria.

He told The Independent on Sunday: "These chemicals have the ability to cause severe damage to DNA in the mitochondria to the point that they totally inactivate it: they knock it out altogether.

"The mitochondria consumes the oxygen to give you energy and if you damage it - as happens in a number if diseased states - then the cell starts to malfunction very seriously. And there is a whole array of diseases that are now being tied to damage to this DNA - Parkinson's and quite a lot of neuro-degenerative diseases, but above all the whole process of ageing."

Science Daily — Parkinson's disease is well-known for its progression of motor disorders: stiffness, slowness, tremors, difficulties walking and talking. Less well known is that Parkinson's shares other symptoms with narcolepsy, a sleep disorder characterized by sudden and uncontrollable episodes of deep sleep, severe fatigue and general sleep disorder.

Now a team of UCLA and Veterans Affairs researchers think they know why — the two disorders share something in common: Parkinson's disease patients have severe damage to the same small group of neurons whose loss causes narcolepsy. The findings suggest a different clinical course of treatment for people suffering with Parkinson's that may ameliorate their sleep symptoms.

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have determined that Parkinson's disease patients have a loss of up to 60 percent of brain cells containing the peptide hypocretin.

In 2000, this same group of UCLA researchers first identified the cause of narcolepsy as a loss of hypocretin, thought to be important in regulating the sleep cycle. This latest research points to a common cause for the sleep disorders associated with these two diseases and suggests that treatment of Parkinson's disease patients with hypocretin or hypocretin analogs may reverse these symptoms.

More than 1 million people in the U.S. have been diagnosed with Parkinson's disease, and approximately 20 million worldwide. (The percentage of those afflicted increases with age.) Narcolepsy affects approximately one in 2,000 individuals — about 150,000 in the United States and 3 million worldwide. Its main symptoms are sleep attacks, nighttime sleeplessness and cataplexy, the sudden loss of skeletal muscle tone without loss of consciousness; that is, although the person cannot talk or move, they are otherwise in a state of high alertness, feeling, hearing and remembering everything that is going on around them.

"When we think of Parkinson's, the first thing that comes to mind are the motor disorders associated with it," said Siegel, who is also chief of neurobiology research at the Sepulveda Veterans Affairs Medical Center in Mission Hills, Calif. "But sleep disruption is a major problem in Parkinson's, often more disturbing than its motor symptoms. And most Parkinson's patients have daytime sleep attacks that resemble narcoleptic sleep attacks."

In fact, said Siegel, Parkinson's disease is often preceded and accompanied by daytime sleep attacks, nocturnal insomnia, REM sleep disorder, hallucinations and depression. All of these symptoms are also present in narcolepsy.This is interesting to me because I have the gene for narcolepsy. I quite coffee for a week, and I was literally stumbling around and banging my head in the morning. Coffee stimulates dopamine production, which is lacking in parkinson's disease. Less dopamine makes you less motivated and makes you more disorganized and impulsive. No comment.

Science Daily — Parkinson's disease is well-known for its progression of motor disorders: stiffness, slowness, tremors, difficulties walking and talking. Less well known is that Parkinson's shares other symptoms with narcolepsy, a sleep disorder characterized by sudden and uncontrollable episodes of deep sleep, severe fatigue and general sleep disorder.

Now a team of UCLA and Veterans Affairs researchers think they know why — the two disorders share something in common: Parkinson's disease patients have severe damage to the same small group of neurons whose loss causes narcolepsy. The findings suggest a different clinical course of treatment for people suffering with Parkinson's that may ameliorate their sleep symptoms.

In their report in the May issue of the journal Brain, Jerry Siegel, professor of psychiatry and biobehavioral sciences at the Semel Institute for Neuroscience and Human Behavior at UCLA, assistant resident neurobiologist Thomas C. Thannickal and associate research physiologist Yuan-Yang Lai have determined that Parkinson's disease patients have a loss of up to 60 percent of brain cells containing the peptide hypocretin.

In 2000, this same group of UCLA researchers first identified the cause of narcolepsy as a loss of hypocretin, thought to be important in regulating the sleep cycle. This latest research points to a common cause for the sleep disorders associated with these two diseases and suggests that treatment of Parkinson's disease patients with hypocretin or hypocretin analogs may reverse these symptoms.

More than 1 million people in the U.S. have been diagnosed with Parkinson's disease, and approximately 20 million worldwide. (The percentage of those afflicted increases with age.) Narcolepsy affects approximately one in 2,000 individuals — about 150,000 in the United States and 3 million worldwide. Its main symptoms are sleep attacks, nighttime sleeplessness and cataplexy, the sudden loss of skeletal muscle tone without loss of consciousness; that is, although the person cannot talk or move, they are otherwise in a state of high alertness, feeling, hearing and remembering everything that is going on around them.

"When we think of Parkinson's, the first thing that comes to mind are the motor disorders associated with it," said Siegel, who is also chief of neurobiology research at the Sepulveda Veterans Affairs Medical Center in Mission Hills, Calif. "But sleep disruption is a major problem in Parkinson's, often more disturbing than its motor symptoms. And most Parkinson's patients have daytime sleep attacks that resemble narcoleptic sleep attacks."

In fact, said Siegel, Parkinson's disease is often preceded and accompanied by daytime sleep attacks, nocturnal insomnia, REM sleep disorder, hallucinations and depression. All of these symptoms are also present in narcolepsy.

Science Daily — The case for low-carbohydrate diets is gaining weight. Researchers at the Stanford University School of Medicine have completed the largest and longest-ever comparison of four popular diets, and the lowest-carbohydrate Atkins diet came out on top.

"Many health professionals, including us, have either dismissed the value of very-low-carbohydrate diets for weight loss or been very skeptical of them," said lead researcher Christopher Gardner, PhD, assistant professor of medicine at the Stanford Prevention Research Center. "But it seems to be a viable alternative for dieters."

Of the more than 300 women in the study, those randomly assigned to follow the Atkins diet for a year not only lost more weight than the other participants, but also experienced the most benefits in terms of cholesterol and blood pressure.

"Many health professionals, including us, have either dismissed the value of very-low-carbohydrate diets for weight loss or been very skeptical of them," said lead researcher Christopher Gardner, PhD, assistant professor of medicine at the Stanford Prevention Research Center. "But it seems to be a viable alternative for dieters."

Science Daily — Scientists say that low carbohydrate diets, like the Atkins and South Beach Diets, may actually be the best option for men who want to slim. New research, published this week in the Open Access journal, Nutrition & Metabolism, shows that over 70% of men lost more weight and fat on a low carbohydrate diet, despite eating more calories.

Jeff Volek and colleagues, from the University of Connecticut, also show for the first time that a low carbohydrate diet is much more effective in losing fat from the stomach and chest. Upper body fat carries "a greater health risk than fat stored in other regions of the body," say the authors. They found that fat loss in men was three-times greater in the trunk area, when they were on a low-carbohydrate regime compared to the low-fat diet. Nearly all participants in the study (12 of 15 men and 12 of 13 women) lost more fat on their upper body on the low- carbohydrate diet.

belly fat is strongly associated with diabetes, insulin resistance, heart disease, and all the bad things of syndrome X.

Science Daily — A modified version of a popular low-carbohydrate, high-fat diet is nearly as effective at controlling seizures as the highly restrictive ketogenic diet, Johns Hopkins Children's Center researchers report.

"Our findings suggest relatively good efficacy compared to the ketogenic diet," said Eric Kossoff, M.D., a pediatric neurologist at Johns Hopkins Children's Center. "With 20 patients, our study wasn't large enough to say patients and physicians should replace the proven, but highly restricted ketogenic diet, but the results are encouraging and intriguing."

The common elements in both the ketogenic and Atkins diets are relatively high fat and low carbohydrate foods that alter the body's chemistry. The ketogenic diet mimics some of the effects of starvation, in which the body first uses up glucose and glycogen before burning stored body fat. In the absence of glucose, the body produces ketones, a chemical by-product of fat that can inhibit seizures. Children who remain seizure-free for two years on the ketogenic diet often can resume normal eating without the return of seizures.

The modified Atkins diet is better tolerated by children and may be easier for parents and children to follow, said Kossoff, who presented the study's findings today in Washington, D.C. at a meeting of the American Epilepsy Society.

The findings, which appear the April issue of the Journal of Experimental Medicine, suggest that manipulating IL-25 could provide a method to treat a wide variety of chronic inflammatory diseases.

"It appears that IL-25 has a Jekyll and Hyde personality: it can be helpful or hurtful depending on how it interacts with T helper cells, a subset of immune cells that influences inflammatory responses," said David Artis, an assistant professor in Penn's Department of Pathobiology and senior author of the study. "These studies show that IL-25 promotes type 2 T helper cells that drive the type of response required for eradicating worm infections and causing asthma. Importantly, IL-25 can simultaneously limit destructive inflammation caused by inflammatory T helper cells commonly found in diseases like inflammatory bowel disease, arthritis and MS."

IL-25 can be considered a "good" cytokine by limiting chronic inflammatory responses. At the same time, the ability of IL-25 to promote type 2 responses that drive asthma could be considered the "evil" side of the cytokine.

By examining mice infected with Trichuris, a species of intestinal parasites known as whipworms, the researchers were able to define IL-25's role in promoting type 2 inflammation to fight infection. In mice that lack the ability to produce IL-25, researchers saw a dramatic reduction in the ability to mount a type 2 response that eradicates the parasites. Furthermore, in the absence of IL-25, mice developed a destructive inflammatory response similar to that observed in models of inflammatory bowel disease.

These results also support the notion that the immune response that causes allergies and asthma is an evolutionary hangover resulting from mankind's historical fight with parasitic worm infections. That is, a type 2 response that was once useful in fighting worm infections has now become a dangerous menace, causing inflammatory responses to commonly encountered environmental antigens. About 30 percent of Americans suffer from the negative affects of type 2 inflammation: asthma and allergies. These conditions result from an inflammatory response to factors encountered in the environment, whether they are industrial air pollutants or molecules of peanut oil.

"It is possible that for most of human history, cytokines like IL-25 have promoted type 2 T helper cells that fight infection with intestinal parasites like Trichuris, " said Colby Zaph, a co-author and Irvington Research Fellow at Penn. "In industrialized countries, where worm infections are now rare, this redundant type 2 response is associated with diseases like asthma. "Identifying a role for IL-25 in this type of response may offer an exciting new avenue for treating diseases associated with dysregulated inflammatory responses," Zaph said.